Ketoconazole에 의한 간염 1예

임양희,이은령,문일환 梨花女子大學校 醫科大學 醫科學硏究所 1987 EMJ (Ewha medical journal) Vol.10 No.1

Ketoconazole-induced hepatitis was found in 36-year-old woman who developed easy fatiguability and jaundice, with abnormal liver function tests after taking ketoconazole 400mg a day for 6 months. All of the viral hepatitis serologic markers were negarive. Clinical and biochemical abnormalities spontaneously improved within 3 weeks after cessation of drug administration.

레닌보다 푸쉬킨을 숭배하는 예술혼

임양희 샘터사 1995 월간 샘터 Vol.26 No.8

골격성 제 Ⅲ급 부정교합 환자의 상하악 동시이동술시 LeFort Ⅰ 상악골절단술의 술후 안정성에 관한 연구

임양희,고승오,신효근 大韓口腔外科學會 2003 大韓口腔外科學會誌 Vol.27 No.5

화훼장식 교육에서 색채에 관한 교수자와 학습자의 인식

임양희(Yang Hee Lim),이화은(Hwa Eun Lee),홍종원(Jong Won Hong),박천호(Chun Ho Pak) 한국원예학회 2009 한국원예학회 학술발표요지 Vol.2009 No.5

급성 맹장염에 과한 임상적 및 병리조직학적 연구

박성숙,임양희 이화여자대학교 의과대학 1982 梨花醫學誌 Vol.- No.14

The clinical and histopathological findings, and leukocytes count in 164 patients with acute appendicitis were studied. And results were as follows: 1) In age distribution, most of the acute appendicitis occurred in young adults. 2) In sex distribution, the ratio of female to male was 1.5:1. 3) The most common clinical symptom was abdominal pain, and the chief complaints were nausea, vomitting, etc. Most of the patients came to hospital within one day from its onset of symptom. 4) In WBC count of peripheral blood, the most frequent value was 5000∼15000 per ㎣. 5) The histopathological study showed 53.7% of acute appendicitis with 7.9% of perforation, 1.2% of chronic appendicitis, 22.6% of non-inflammatory findings and 19.5% of no pathologic abnormalities. 6) The possible mechanisms of acute appendicitis present lymphoid hyperplasia, fecalith impaction and dilatation. 7) The accompanying disease of acute appendicitis were 66.7% of mucosal hyperplasia and 33.3% of diverticulum.

회복조기 심근경색환자에서 24시간 Ambulatory 검사에 의한 부정맥의 관찰

손현주,임양희,박성숙,신길자,이우형 대한순환기학회 1986 Korean Circulation Journal Vol.16 No.4

상순의 발생

고승오,임양희,김기병,신효근 대한구순구개열학회 2007 대한구순구개열학회지 Vol.10 No.1

The vertebrate upper lip forms from initially freely projecting maxillary, medial nasal, and lateral nasal prominences at the rostral and lateral boundaries of the primitive oral cavity. These facial prominences arise during early embryogenesis from ventrally migrating neural crest cells in combination with the head ectoderm and mesoderm and undergo directed growth and expansion around the nasal pits to actively fuse with each other. Initial fusion is between lateral and medial nasal processes and is followed by fusion between maxillary and medial nasal processes. Fusion between these prominences involves active epithelial filopodial and adhering interactions as well as programmed cell death. Slight defects in growth and patterning of the facial mesenchyme or epithelial fusion result in cleft lip with or without cleft palate, the most common and disfiguring craniofacial birth defect. This review will summarize the current understanding of the basic morphogenetic processes and molecular mechanisms underlying upper lip development.

류마티스성 심장판막질환, 우심방혈전 및 대동맥 협착증과 합병된 만성 혈전색전성 폐동맥고혈압 1예

유근배,심준,임양희,이진화,신길자 梨花女子大學校 醫科大學 醫科學硏究所 1998 EMJ (Ewha medical journal) Vol.21 No.4

폐동맥 혈전색전증은 비교적 드문 질환으로 주로 심부 정맥혈전에서 발생하는 것으로 알려져 있으며 류마티스성 심장판막질환을 가진 경우 합병되는 우심방 혈전이 드물게 폐혈전색전증의 원인이 될 수 있는데, 저자들은 대동맥의 동맥경화성 협착증을 동반한 류마티스성 심판막질환 환자에서 우심부전 및 우심방혈전에서 발생한 만성 혈전색전성 폐동맥고혈압1예를 경험하였기에 문헌고찰과 함께 보고하는 바이다. Most pulmonary thromboemboli arise from the deep vein thrombosis, which have complete clinical and at least near complete roentgenographic and angiographic resolution within four to six week of the acute event. But chronic pulmonary hypertension and cor pulmonale from unresolved pulmonary embo-lism complicate acute embolic episode with a frequency of less than 1 percent. Rarely pulmo-nary thromboemboli can result from right atrial thrombi. We experienced a case of chronic thromoboembolic pulmonary hypertension, which wrose from right atrial thrombi in the patient with rheumatic valvaular heart disease and thoracic aorta atherosclerotics stenosis.

이차구개 형태분화의 내적 조절유전자 규명

이재국,장은하,임양희,김기병,고승오,조의식,신효근 대한구순구개열학회 2007 대한구순구개열학회지 Vol.10 No.1

이차구개는 발생과정에서 구개선반의 형성과 성장, 거상과 융합의 과정을 통해 형성된다. 이와 같은 이차구개의 형성과정은 미세한 분자유전학적 신호전달기전에 의해 조절되는 것으로 알려져 있어서, 신호전달과정에 관여하는 유전인자의 발현이상이 되면 정상적인 이차구개가 형성되지 못하고 구개파열이라는 선천성 기형이 발생된다. 구개파열의 유발인자들에 대한 많은 연구에도 불구하고 현재까지 정상적인 이차구개의 형성을 조절하는 분자유전학적 기전에 대해서는 명확히 알려져 있지 않다. 따라서 본 연구에서는 이차구개의 형태분화를 조절하는 분자유전학적 기전을 알아보고자, 이차구개 형성의 내적 조절인자 중 핵심유전자로 알려져 있는 Osr 2가 결손된 생쥐의 이차구개 형성과정에서 정상생쥐에 비해 발현의 변동이 나타나는 유전자를 확인하였다. 유전자 발현의 변동은 발생 14.5일(E14.5)의 구개선반으로부터 추출한 total RNA를 이용하여 ACP-based GeneFishing PCR을 시행하여 확인하였고, 각각의 변동된 유전자를 동정하여 정상생쥐의 이차구개 형성과정에서의 발현양상을 insitu hybridization을 시행하여 확인하였다. 총 120쌍의 primer를 이용한 검색을 통해서 정상생쥐의 구개선반에 비해 mutant에서 발현이 변동된 유전자는 7개가 검출되었고, 이들은 모두 정상생쥐에 비해 mutant에서 발현이 증 가되는 것으로 확인되었다. 검출된 유전자는 vimentin(Vim), β-tropomyosin 2(Tpm2 ), thioredoxin-like5(Txnl5 ), procollagen type II alpha 1(Col2a1 ), Insulin-like growth factor binding protein 7(IGFbp7 ), Sui 1 homologs(Sui1 ), Defender against cell death 1(Dad1 )이었다. 검출된 유전자를 동정하여 정상생쥐의 구개 형성과정에서의 발현양상을 알아본 결과, Col2a1 을 제외한 유전자들은 모두 E13.5의 구개선반에서 특이적으로 발현되고 있었으나 구개선반이 융합된 E15.5에서는 Vim, Txnl5 그리고 Dad1 만이 봉합선을 따라 발현이 지속되고 있었다. 이상의 결과로 보아 검출된 유전자들은 구개선반의 형태분화과정에서 발현되어 이차구개의 형성과정에 관여할 것으로 여겨진다. 또한 이들은 이차구개 형성의 내적조절인자인 Osr2의 downstream target으로 구개선반의 성장과 융합과정에 직접적으로 관여하는 유전물질일 것으로 추정된다.

혈액투석을 받는 만성신부전증 환자의 혈장 Erythropoietin 농도 및 rhEPO 의 효과

이지수,윤견일,임양희,최규복,편욱범 대한신장학회 1992 Kidney Research and Clinical Practice Vol.11 No.4

Baekground: A relative deficiency of erythropoietin has been recognized as the major reason for the anemia accompanying chronic renal failure (CRF). Recently recombinant human erythrepoietin is used as a major therapeutic agent for correcting the anemia of CRF. However the reason why the adaptation of EPO levels to hemoglobin concentration is lost during CRF has not been investigated systematically. In this study we sought the mechanism of EPO deficiency and the possibility of EPO resistance. Methods: We studied the relationship between plasma erythropoietin level and other variables in 3 subgroups of CRF patients undergoing maintenance hemodialysis and control groups with normal renal function. We measured plasma erythropoietin, PTH levels by radioimmunoassay and plasma aluminum level by photometry. Results: In control group (n=10), plasma erythropoietin level (16.02?2.47mU/ml) was higher than in cystic disease and hemodialysis-only group (p<0.01). Plasma erythropoietin level in erythropoietin-treated group (n=7, 12.34+-9.34mU/ml) was significantly higher than in hemodialysis-only group (n=48, 4.63+-4. 90 mU/ml) (p < 0. 05), but there was no significant difference in hematocrit between two groups (25.06?2.939mg, 23.09?4-5.1896 respectively). However hematocrit was significantly increased after erythropoietin treatment (from 18.40? 3.12% to 25.06?2.939%, p<0.01). In cystic disease group (n=4, including 1 poycystic kidney disease & 3 ACKD), plasma erythropoietin level (7.50+-0. 55 mU/ml) and hematocrit (31.87+-3.839,) were significantly higher than in hemodialysis-only group (p<0.01, p<0.05 respectively). There was no difference in plasma erythropoietin level between erythropoietin- treated group and cystic disease group, but hematocrit was higher in cystic disease group than erythropoietin- treated group (p<0.05). There was no relation between plasma erythropoietin and plasma PTH level in all groups. In erythropoietin-treated group, there was also no relation between hematocrit change and plasma aluminum level. Only in cystic disease group, there was strong positive relation between plasma erythropoietin level and hematocrit (r=0.9134, p<0.05). Conclusion: We could find the fact that it may not be the capability to produce EPO but rather the adaptation of EPO production to the hemoglobin concentration (namely, oxygen sensor function) that is disturbed during CRF. Also we could not discard the possibility of EPO resistance in CRF.